Epilepsia
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Epileptogenesis refers to a phenomenon in which the brain undergoes molecular and cellular alterations after a brain-damaging insult, which increase its excitability and eventually lead to the occurrence of recurrent spontaneous seizures. Common epileptogenic factors include traumatic brain injury (TBI), stroke, and cerebral infections. Only a subpopulation of patients with any of these brain insults, however, will develop epilepsy. ⋯ Animal models of epileptogenesis are therefore necessary for scientific progress. Recent advances in the development of experimental models of epileptogenesis have provided tools to investigate the molecular and cellular alterations and their temporal appearance, as well as the epilepsy phenotype after various clinically relevant epileptogenic etiologies, including TBI and stroke. Studying these models will lead to answers to critical questions such as: Do the molecular mechanisms of epileptogenesis depend on the etiology? Is the spectrum of network alterations during epileptogenesis the same after various clinically relevant etiologies? Is the temporal progression of epileptogenesis similar? Work is ongoing, and answers to these questions will facilitate the identification of molecular targets for antiepileptogenic treatments, the design of treatment paradigms, and the determination of whether data from one etiology can be extrapolated to another.
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Weight gain or loss is not an integral part of epilepsy although a sedentary lifestyle can contribute to weight gain. Pharmacological treatment for epilepsy may be associated with substantial weight changes that may increase morbidity and impair adherence to the treatment regimen. ⋯ Weight neutral AEDs are lamotrigine, levetiracetam, and phenytoin. In clinical practice it is critical to weigh patients regularly and AED selection should be based on each patient's profile without sacrificing therapeutic efficacy.
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While the treatment of refractory status epilepticus (SE) relies on the use of anesthetic agents, mostly barbiturates, propofol, or midazolam, the study of the available literature discloses that the evidence level is low. Therapeutic coma induction appears straightforward for generalized convulsive or subtle SE, but this approach is debated for complex partial SE. ⋯ However, it seems that the biological background of the patient (especially the etiology) remains the main prognostic determinant in SE. There is a clear need of controlled trials regarding this topic.